STUDY ON THE ETIOPATHOGENESIS OF MULTIPLE SPONGY NECROSIS OF THE PONTINE BASE IN 3 AUTOPSY CASES

Citation
R. Okeda et al., STUDY ON THE ETIOPATHOGENESIS OF MULTIPLE SPONGY NECROSIS OF THE PONTINE BASE IN 3 AUTOPSY CASES, Acta Neuropathologica, 96(2), 1998, pp. 123-128
Citations number
4
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
96
Issue
2
Year of publication
1998
Pages
123 - 128
Database
ISI
SICI code
0001-6322(1998)96:2<123:SOTEOM>2.0.ZU;2-#
Abstract
The etiopathogenesis of multiple spongv necrosis (MSN) of the pontine base was analyzed by examining the spatial relationship with intra- an d extrafascicular vascular structures by reconstruction of serial sect ions of nine lesions from three autopsy cases. All nine lesions in the fascicles were distributed without any spatial relationship to the in trafascicular vessels. Instead, these lesions were distributed in para llel with arterial and venous transverse main branches between the ant eromedial and anterolateral groups of the pontine vessels. On the othe r hand, all lesions in the middle cerebellar peduncle were arranged ob liquely along the arterial and venous main trunks of the lateral group vessels with sparing of the perivascular narrow zone of the white mat ter. Moreover, narrow fascicles, even though located in the dorsomedia l region of the pontine base, which is consistently involved in MSN, w ere spared, and thick transverse and longitudinal fascicles were selec tively involved. The marginal zone of fascicles was spaced, and focal coagulation necrosis was sometimes found in MSN lesions. Additionally, normal fascicles did not have their own nutritional arteries, and wer e nourished by arterioles and capillaries from the surrounding pontine gray matter. Neither severe organic stenosis nor occlusion of pontine vessels was found. On the basis of the close topographical relationsh ip of MSN lesions with the pontine vascular architecture in addition t o preferential involvement of thick fascicles with sparing of the marg inal zone and inclusion of focal coagulation necrosis, it is proposed that the etiopathogenesis of MSN is pontine ischemia on a background o f the characteristic parenchymal and vascular architecture of the pont ine base. As to the cause of the ischemia, it is proposed that some fu nctional disorder such as arterial vasoconstriction in the pontine bas e or the vertebrobasilar artery is responsible, rather than organic ch anges in the vessles.